Osmoregulatory bicarbonate secretion exploits H(+)-sensitive haemoglobins to autoregulate intestinal O2 delivery in euryhaline teleosts.

Osmoregulatory bicarbonate secretion exploits H(+)-sensitive haemoglobins to autoregulate intestinal O2 delivery in euryhaline teleosts.
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DOI:
10.1007/s00360-014-0844-x
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发表时间:
2014-10
期刊:
Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology
影响因子:
--
通讯作者:
Wilson RW
Wilson RW
中科院分区:
其他
文献类型:
--
作者:
Cooper CA;Regan MD;Brauner CJ;De Bastos ES;Wilson RW

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海洋硬骨鱼分泌碳酸氢盐(HCO3−)进入肠道,以帮助渗透调节和限制碳酸氢盐沉淀对Ca2+的吸收。肠道HCO3−的分泌与质子(H+)进入血液的等摩尔运输有关,两者都与环境盐度成正比。我们假设海水硬骨鱼对H+敏感的血红蛋白(Hb)系统可以通过玻尔效应和/或根效应(降低Hb-O2亲和力和/或随pH降低的能力)来改善与渗透调节相关的高代谢需求时肠细胞对O2的输送。为了验证这一点,我们表征了欧洲比目鱼(Platichthys flesus)血红蛋白的H+平衡和气体交换特性,并构建了一个模型,将这些值、肠血流量和三种不同环境盐度(33、60和90)下的动静脉酸化结合起来。该模型表明,红细胞pH值(pHi)在通过肠道毛细血管时可以降低0.14-0.33个单位(取决于外部盐度),这足以激活玻尔效应(玻尔系数为- 0.63),甚至可能激活根效应,并在不改变血流的情况下提高组织O2输送高达42%。在活体中无法测量比目鱼的肠道静脉血pH值,但在适应海水的虹鳟鱼中,证实了血液酸化不小于0.2单位(相当于pHi的- 0.12)。当使用鳟鱼特异性值作为模型变量时,预测值与体内测量值一致,进一步支持了模型。因此,该系统是一个自我调节的优雅例子:在较高的环境盐度下,随着对昂贵的渗透调节过程(包括HCO3−分泌)的需求增加,通过局部酸中毒和玻尔(可能还有根)效应向肠道输送氧气的增强也是如此。
Marine teleost fish secrete bicarbonate (HCO3 −) into the intestine to aid osmoregulation and limit Ca2+ uptake by carbonate precipitation. Intestinal HCO3 − secretion is associated with an equimolar transport of protons (H+) into the blood, both being proportional to environmental salinity. We hypothesized that the H+-sensitive haemoglobin (Hb) system of seawater teleosts could be exploited via the Bohr and/or Root effects (reduced Hb-O2 affinity and/or capacity with decreasing pH) to improve O2 delivery to intestinal cells during high metabolic demand associated with osmoregulation. To test this, we characterized H+ equilibria and gas exchange properties of European flounder (Platichthys flesus) haemoglobin and constructed a model incorporating these values, intestinal blood flow rates and arterial–venous acidification at three different environmental salinities (33, 60 and 90). The model suggested red blood cell pH (pHi) during passage through intestinal capillaries could be reduced by 0.14–0.33 units (depending on external salinity) which is sufficient to activate the Bohr effect (Bohr coefficient of −0.63), and perhaps even the Root effect, and enhance tissue O2 delivery by up to 42 % without changing blood flow. In vivo measurements of intestinal venous blood pH were not possible in flounder but were in seawater-acclimated rainbow trout which confirmed a blood acidification of no less than 0.2 units (equivalent to −0.12 for pHi). When using trout-specific values for the model variables, predicted values were consistent with measured in vivo values, further supporting the model. Thus this system is an elegant example of autoregulation: as the need for costly osmoregulatory processes (including HCO3 − secretion) increases at higher environmental salinity, so does the enhancement of O2 delivery to the intestine via a localized acidosis and the Bohr (and possibly Root) effect.
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